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        Magnesium isoglycyrrhizinate inhibits L-type Ca2+ channels, Ca2+ transients, and contractility but not hERG K+ channels

        Yue Lin,Yuanyuan Zhang,Qiongtao Song,Tao Song,Xue Han,Ying Zhang,Xuan Zhang,Xi Chu,Fenghua Zhang,Li Chu,Jianping Zhang 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.10

        To explore the cardiovascular protective effectsof Magnesium isoglycyrrhizinate (MI), especially theunderlying cellular mechanisms related to L-type calciumchannels and myocardial contractility, and to examine theeffects of MI on hERG K? current expressed in HEK293cells. We used the whole-cell patch clamp technique,video-based edge detection and dual excitation fluorescencephotomultiplier systems to explore the effect of MIon L-type Ca2? currents (ICa-L) and cell contraction in ratcardiomyocytes. We also examined the rapidly activatingdelayed rectifier potassium current (IKr) expressed inHEK293 cells using a perforated patch clamp. MI inhibitedICa-L in a dose-dependent manner, with a half-maximalinhibitory concentration (IC50) of 0.22 mg/ml, and themaximal inhibitory effect was 61.10 ± 0.59%. MI at aconcentration of 0.3 mg/ml reduced cell shortening by24.12 ± 3.97% and the peak value of the Ca2? transient by36.54 ± 4.96%. MI had no significant influence on hERGK? channels expressed in HEK293 cells at all testpotentials. MI exerts protective effects on the heart via theinhibition of ICa-L and cell shortening in rat cardiomyocytes. However, MI had no significant influence on IKr;thus, MI may exert cardioprotective effects without causingdrug-induced long QT syndrome.

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